Diabetic Retinopathy: Understanding Pathologic Angiogenesis and Exploring its Treatment Options

ABSTRACT

Diabetic retinopathy is the major cause of blindness at working age. The pathogenesis behind visual loss is related with retinal angiogenesis and increased retinal vascular permeability. These changes seem to be the result of chronic hyperglycemia and hypoxia. Several mechanisms have been proposed to cause the retinal and vasculature cellular damage. They include the formation of advanced end glycation products, aldose reductase activity and reactive oxygen species. Ultimately, they lead to the expression of VEGF-A. This growth factor seems to play the pivotal role in the development of the complications associated with the disease including break down of the inner blood retinal barrier, macular edema and vasoproliferation. Other mechanisms like inflammation, protein kinase C activity and erythropoietin have been strongly associated with the pathogenesis.

Laser therapy is still the standard of care for diabetic retinopathy and prevents severe vision loss in 95% of patients if timely treatment is performed. The better understanding of the disease has led to the production of new management options that may become important adjuvants for the disease. They include intravitreal anti-VEGF therapy, intravitreal steroid therapy and systemic protein kinase C inhibitors. Vitrectomy is an important option for advanced cases of the disease such as tractional retinal detachment or non-absorbing vitreous hemorrhages.

Keywords:

Angiogenesis, proliferative diabetic retinopathy, diabetic macular edema, intravitreal anti-VEGF therapy, intravitreal corticosteroid therapy.